Among the thousands of bacterial species contained within the intestinal gut flora, it is accepted that each species requires the use of adhesin proteins, or some combination thereof, that bring the bacteria closer to the epithelia and allow them to colonize the intestine. In a similar way, enteric pathogens also require surface-localized adhesins for colonization of the host intestine and eventual establishment of disease. Enterohemorrhagic Escherichia coli (EHEC) and, in general, Shiga toxin-producing E. coli (STEC) strains are known to contain a large number of proteins responsible for adhesion and contribute to establishment, persistence, and tissue tropism observed during infection with these pathogens. Understanding how these adhesins work is critical to having a full picture of the pathogenic and pathophysiological process associated with EHEC. Further, because adhesins play such an important role in virulence, they are targets for therapeutic intervention. Thus, this review summarizes the current knowledge on the adhesive proteins in EHEC, emphasizing up-to-date information and discussing gaps in knowledge and future directions in the study of these virulence factors.

Time line and proposed roles of major fimbrial/afimbrial adhesin proteins in EHEC. In (A), Lpf is interacting with the extracellular membrane (ECM) proteins, such as laminin, collagen IV, and fibronectin. After the initial interaction with the intestine is established, EHEC is able to closely attach to the host cell (B) through an interaction of the surface protein intimin with the translocated receptor protein Tir and nucleolin. In (C), the interaction between Tir and intimin is established, initiating a host-cell actin rearrangement via participation of the translocated bacterial protein EspFu and the recruitment of several host proteins. In (D), ECP and HCP are proposed to interact with the surface of host intestinal cells, perhaps strengthening the colonization through the formation of microcolonies and/or biofilms. Further, curli is shown to contribute in the establishment of biofilms, though an interaction with ECP and HCP is not demonstrated. Finally in (E), dominant curli expression has been proposed as detrimental for the survival of EHEC in the intestine, suggesting that this surface structure might become important for the pathogen interaction with abiotic surfaces and during colonization of the surface of vegetable and plant leaves. doi:10.1128/microbiolspec.EHEC-0003-2013.f2

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Figure 2

Time line and proposed roles of major fimbrial/afimbrial adhesin proteins in EHEC. In (A), Lpf is interacting with the extracellular membrane (ECM) proteins, such as laminin, collagen IV, and fibronectin. After the initial interaction with the intestine is established, EHEC is able to closely attach to the host cell (B) through an interaction of the surface protein intimin with the translocated receptor protein Tir and nucleolin. In (C), the interaction between Tir and intimin is established, initiating a host-cell actin rearrangement via participation of the translocated bacterial protein EspFu and the recruitment of several host proteins. In (D), ECP and HCP are proposed to interact with the surface of host intestinal cells, perhaps strengthening the colonization through the formation of microcolonies and/or biofilms. Further, curli is shown to contribute in the establishment of biofilms, though an interaction with ECP and HCP is not demonstrated. Finally in (E), dominant curli expression has been proposed as detrimental for the survival of EHEC in the intestine, suggesting that this surface structure might become important for the pathogen interaction with abiotic surfaces and during colonization of the surface of vegetable and plant leaves. doi:10.1128/microbiolspec.EHEC-0003-2013.f2

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